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严重张力性气胸对猪模型的生理学和心血管效应。

Physiology and cardiovascular effect of severe tension pneumothorax in a porcine model.

机构信息

Deptartment of Surgery, Madigan Army Medical Center, Fort Lewis, Washington, USA.

出版信息

J Surg Res. 2013 Sep;184(1):450-7. doi: 10.1016/j.jss.2013.05.057. Epub 2013 Jun 5.

Abstract

BACKGROUND

Pneumothoraces are relatively common among trauma patients and can rapidly progress to tension physiology and death if not identified and treated. We sought to develop a reliable and reproducible large animal model of tension pneumothorax and to examine the cardiovascular effects during progression from simple pneumothorax to tension pneumothorax.

MATERIALS AND METHODS

Ten swine were intubated, sedated, and placed on mechanical ventilation. After a midline celiotomy, a 10-mm balloon-tipped laparoscopic trocar was placed through the diaphragm, and a 28F chest tube was placed in the standard position and clamped. Thoracic insufflation was performed in 5-mm increments, and continuous cardiovascular measurements were obtained.

RESULTS

Mean insufflation pressures of 10 mm Hg were associated with a 67% decrease in cardiac output (6.6 L/min versus 2.2 l/min; P = 0.04). An additional increase in the insufflation pressure (mean 15 mm Hg) was associated with an 82% decrease in cardiac output from baseline (6.8 versus 1.2 L/min; P < 0.01). Increasing insufflation pressures were associated with a corresponding increase in central venous pressure (from 7.6 mm Hg to 15.2 mm Hg; P < 0.01) and a simultaneous decrease in the pulmonary artery diastolic pressure (from 15 mm Hg to 12 mm Hg; P = 0.06), with the central venous pressure and pulmonary artery diastolic pressure approaching equalization immediately before the development of major hemodynamic decline. Pulseless electrical activity arrest was induced at an average of 20 mm Hg. Tension physiology was immediately reversible with adequate decompression, allowing for multiple repeated trials.

CONCLUSIONS

A reliable and highly reproducible model was created for severe tension pneumothorax in a large animal. Major cardiovascular instability proceeding to pulseless electrical activity arrest with stepwise insufflation was noted. This model could be highly useful for studying new diagnostic and treatment modalities for tension pneumothorax.

摘要

背景

气胸在创伤患者中较为常见,如果未能及时发现和治疗,可能迅速发展为张力性气胸,并导致生理张力和死亡。我们试图建立一种可靠且可重复的大型动物张力性气胸模型,并研究从单纯气胸发展为张力性气胸过程中的心血管效应。

材料和方法

10 头猪进行气管插管、镇静和机械通气。开腹后,通过膈肌插入 10mm 球囊尖端腹腔镜trocar,标准位置插入 28F 胸腔引流管并夹闭。每次递增 5mm 进行胸腔充气,并持续进行心血管测量。

结果

平均充气压力为 10mmHg 时,心输出量降低 67%(6.6L/min 降至 2.2L/min;P=0.04)。进一步增加充气压力(平均 15mmHg),心输出量较基线降低 82%(6.8 降至 1.2L/min;P<0.01)。充气压力增加与中心静脉压相应增加(从 7.6mmHg 升至 15.2mmHg;P<0.01)以及肺动脉舒张压同时降低(从 15mmHg 降至 12mmHg;P=0.06)相关,在主要血流动力学下降发生前,中心静脉压和肺动脉舒张压接近平衡。平均在 20mmHg 时发生无脉性电活动骤停。充分减压可立即逆转张力性生理,允许进行多次重复试验。

结论

在大型动物中创建了一种可靠且高度可重复的严重张力性气胸模型。随着逐步充气,出现了严重的心血管不稳定,直至无脉性电活动骤停。该模型对于研究张力性气胸的新诊断和治疗方法可能非常有用。

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